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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: J Mol Cell Cardiol. 2019 Feb 15;129:69–78. doi: 10.1016/j.yjmcc.2019.02.009

Figure 6. Reducing ROS damage in GCN5L1 cKO hearts restores post-ischemic functional recovery.

Figure 6.

(A, B) +dP/dt and −dP/dt recovery from I/R injury is restored in GCN5L1 cKO mice in the presence of ROS-scavenger N-acetyl cysteine (NAC). (C-E) Recovery after reperfusion in the presence of NACasa percentage of +dP/dt, −dP/dt, and workload. (F) Infarct volume is reduced three-fold in cKO mice in the presence of NAC following I/R injury, and is no longer significantly different from wildtype mice. (G-I) Changes in post-ischemic function relative to untreated hearts from Figure 3. N = 5 mice per group. ** = P < 0.01, *** = P < 0.001, **** = P <0.0001 vs. WT.